Severe chronic cardiac insufficiency arising from cardiac disease or injury shortens and degrades the quality of life of many patients. One form of severe chronic cardiac insufficiency, congestive heart failure, is a pathophysiological state in which cardiac output is inadequate to meet physiological requirements of the body. The mortality rate for congestive heart failure is greater than 50% within 5 years of onset. Treatments for severe chronic cardiac insufficiency include heart transplants, artificial heart implants and cardiomyoplasty. Cardiac transplantation, using cyclosporine to inhibit tissue rejection, is a very successful technique for prolonging a cardiac patient's life, improving the survival rate to 80% at 1 year. However, the transplant operation is very expensive and heart availability is limited. The artificial heart has had very limited success.
Dynamic cardiomyoplasty is a surgical and electrical therapeutic technique in which a skeletal muscle flap is dissected from a patient, while maintaining its innervating neural tissues and neurovascular structures, and surgically placed around the patient's heart. An electrical stimulation device with an electrical pulse generator and intramuscular electrodes is implanted which performs muscle electrical stimulation in synchrony with ventricular systole to support cardiac pumping.
Stimulated skeletal muscle transforms into a fatigue-resistant state suitable for chronic ventricular assistance, enabling dynamic cardiomyoplasty. This permits substitution of skeletal muscle for a patient's ailing heart muscle. The skeletal muscle is then trained to function in the manner of cardiac muscle to increase the patient's cardiac output. Sequential and progressive skeletal muscle electrical stimulation causes glycolytic muscle fibers, predominant in skeletal muscle, to take the form of oxidative fibers. Oxidative fibers are resistant to fatigue and have histochemical and biochemical characteristics of myocardium.
G. J. Magovern, in U.S. Pat. No. 4,791,911, entitled "Method of Cardiac Reconstructive Surgery", issued Dec. 20, 1988, discloses a surgical method of reconstructing damaged cardiac muscle using a latissimus dorsi skeletal muscle autograft.
U.S. Pat. No. 4,411,268 to J. A. Cox, entitled "Muscle Stimulator," which issued Oct. 25, 1983, describes a pulse generator which delivers conditioning and stimulating pulses to a cardiac muscle graft. These pulses are delivered in synchrony with either the delivery of stimulating pulses to the heart or the sensing of natural heartbeats.
Further detail on the muscle stimulator technique and intracardiac leads for practicing cardiomyoplasty are described in U.S. Pat. No. 4,735,205, by J. C. Chachques et al., entitled "Method and Apparatus Including a Sliding Insulation Lead for Cardiac Assistance", issued Apr. 5, 1988.
Cardiac arrhythmias create one problem that arises with the muscle stimulation techniques. Patients with severe chronic cardiac insufficiency are susceptible to serious arrhythmias. One such arrhythmia is a tachycardia. Cardiac tissue is susceptible to tachycardia episodes if two conditions occur. First, more than one electrical impulse pathway through the heart exists to allow for the presence of circus movement. Second, conduction times and refractory periods within the multiple pathways must be different. One characteristic of reentrant tachycardias is that the cardiac tissue ahead of the impulse is not refractory, allowing the tachycardia to perpetuate itself, and the cardiac tissue behind the impulse is variable or inconsistent with respect to refractory nature. The tissue damage inherent in cases of severe chronic cardiac insufficiency and congestive heart failure promotes the conditions associated with a tachycardia-susceptible cardiac state.
Antitachycardia pacers, cardioverters and defibrillators have been developed to detect arrhythmia episodes and generate an electrical stimulation therapy to terminate such episodes.
Antitachycardia pacers terminate reentrant tachycardias by delivering an electrical stimulation pulse to the heart while cardiac tissue is in a refractory state. The pulse is exactly timed to interrupt a reentrant circuit so that the anterograde limb of the circuit is refractory (so that the tachycardia is not merely reset) and, at the same time, the retrograde limb is rendered refractory. Correct stimulation timing creates electrical charge propagation which penetrates both circuit limbs, interrupting the tachycardia in the one limb and failing to perpetuate the impulse through the other (anterograde) limb, which the impulse cannot enter because the portion of the circuit is refractory. Each of the three forms of antitachycardia pacing--underdrive, overdrive and refractory pacing (also called "extrastimulus pacing")--are attempts to find this correct stimulation timing.
Underdrive pacing is pacing at a rate which is slower than the rate of a tachycardia. Overdrive pacing occurs at a rate which is faster than the tachycardia rate. One problem with underdrive and overdrive pacing is that pulses are delivered asynchronously with respect to the natural impulse propagation of the tachycardia. A long period of therapy may be required before the appropriate stimulus is delivered. Furthermore, these asynchronous methods do not allow the delivery of several successive appropriately timed stimuli. Most importantly, there exists a risk of generating a stimulus pulse during a time when the heart is vulnerable to aggravation of the tachycardia, possibly leading to fibrillation and sudden death.
Dual-demand antitachycardia pacing reduces some of the risk of aggravating an existing tachycardia by providing for automatic tachycardia recognition prior to initiating asynchronous competitive pacing. Only if the antitachycardia therapy is successful and the tachycardia is broken does the dual-demand pacer revert to normal demand pacing.
Further improvement is provided in a dual-chamber antitachycardia device which performs asynchronous competitive pacing (DOO pacing) which doubles the probability of offering an appropriately timed stimulus into the reentrant circuit.
Other, more recent, antitachycardia pacers provide for faster reversion of tachycardias by pacing using a technique of systematic scanning of diastole with single or double impulses, rather than pacing in an asynchronous manner.
Most recently, it was recognized that single impulses sometimes fail to terminate the tachycardia because the areas of refractoriness are interposed between the impulse and the reentrant circuit. An improved antitachycardia pacer employs multiple bursts of rapid impulses to reduce refractoriness and allow entry into the tachycardia circuit. One problem with burst pacing is the increased possibility of pacing during a vulnerable period, leading to tachycardia acceleration and fibrillation. Burst pacers may not be appropriate for automatic, implanted pacing.
In general, antiarrhythmia pacing techniques are not always successful and there is the ever present risk of inducing or aggravating unwanted and possibly dangerous arrhythmias. Present day antitachycardia pacers cannot avoid the delay before initiating therapy which is required for tachycardia detection, recognition and application of treatment. This delay may allow autonomic nervous system sensors within the body to become stimulated, allowing sympathetic nerve activation which raises the heart rate and further alters the refractory nature of cardiac tissue, thereby rendering tachycardia termination more difficult.
Furthermore, it is impossible for antitachycardia pacers to immediately sense that a pacing therapy was successful, causing a delay in terminating the applied therapy. Delivery of unnecessary therapy pulses after a previous extrastimulus pulse has terminated a tachycardia may cause its reinitiation.
A better understanding of the physiological processes underlying the genesis and aggravation of cardiac arrhythmias may lead to an improved treatment for arrhythmia prevention and termination. One such physiological process involves severely reduced blood flow to the heart muscle, called myocardial ischemia. Evidence shows that ischemia causes arrhythmias, including tachycardias and fibrillation, and may lead to sudden cardiac death. Ischemia generates ventricular arrhythmias by way of three main mechanisms. First, ischemia cause automaticity of the myocardial tissue. Automaticity is the propensity to initiate and generate spontaneous ectopic action potentials. Second, the heart develops reentrant circuits via electrical heterogeneity. Here, conduction of action potentials slows in particular ischemia-damaged areas of the heart, resulting in the development of reentry and re-excitation of electrical impulses within the cardiac tissues. Finally, abnormalities of repolarization, such as early and late after-depolarizations further aggravate ventricular arrhythmias. This occurs because, throughout the heart, a variable lengthening or shortening of the refractory periods causes an increased dispersion of refractoriness between ischemic and nonischemic zones.
In this manner, ischemia causes a ventricular tachycardia, in which insufficient time between heartbeats is allowed for diastolic filling. Thus, cardiac output will fall, further aggravating ischemia and leading to the risk of acute myocardial ischemia. Ischemia predisposes the heart to development of totally disorganized ventricular rhythm, called ventricular fibrillation, in which regular cardiac pumping ceases and sudden cardiac death will develop.
The present invention proposes a therapy for preventing and terminating cardiac arrhythmias which may lead to ventricular fibrillation and sudden death in patients suffering from congestive heart failure. The proposed therapy combines antiarrhythmia pacing of various forms with skeletal muscle graft stimulation. Muscle graft stimulation increases cardiac output, aortic pressure and, therefore, perfusion of the heart to alleviate myocardial ischemia and ameliorate arrhythmias.
One group of prior art cardiac assist devices, antiarrhythmia pacing systems, employs electrical stimulus generation to treat cardiac arrhythmias. (See, e.g., U.S. Pat. No. 4,390,021 to R. A. J. Spurrell et al., which issued Jun. 28, 1983, and is entitled "Two Pulse Tachycardia Control Pacer"). Another group of prior art devices, skeletal muscle stimulators (also called "cardiomyostimulators"), utilizes muscle fiber stimulation to elevate cardiac output. (See e.g., U.S. Pat. No. 4,735,205 to J. C. Chachques et al., discussed earlier). While each of the foregoing devices provides satisfactory assistance in its intended therapy area, the therapy provided is insufficient with respect to the therapy area that the other device treats.
It is therefore a primary object of the present invention to provide a method and apparatus for detecting and treating various cardiac arrhythmias, in which treatment a combined antiarrhythmia therapy and skeletal muscle stimulation therapy is provided to terminate the arrhythmia.
Another object of the present invention is to improve the success rate of arrhythmia termination while decreasing the risks of aggravating arrhythmias which may occur when only heart pacing therapies are utilized.
An additional object of the present invention is to increase cardiac perfusion during arrhythmia episodes to ameliorate ischemia and avoid aggravation of the arrhythmia into a more dangerous form.
Further objects and advantages of the present invention will become apparent as the following description proceeds.